ArticleStem cell research & therapy2020
Cellular senescence mediates the detrimental effect of prenatal dexamethasone exposure on postnatal long bone growth in mouse offspring.
Article in Stem cell research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- The protective role of adipogenic lineage precursors in maintaining bone marrow redox homeostasis in a mouse model of prenatal dexamethasone exposure.Redox biology · 2025Article
- The influence of cell source on the senescence of human mesenchymal stem/stromal cells.Human cell · 2025Review
- Senolytic cocktail dasatinib and quercetin attenuates chronic high altitude hypoxia associated bone loss in mice.Scientific reports · 2024Article
- Prenatal dexamethasone exposure reduces osteoprogenitor proliferation in mice via histone modifications at the Mkp-1 gene locus.Communications biology · 2024Article
- LOX overexpression programming mediates the osteoclast mechanism of low peak bone mass in female offspring rats caused by pregnant dexamethasone exposure.Cell communication and signaling : CCS · 2023Article
- Pulsed electromagnetic fields as a promising therapy for glucocorticoid-induced osteoporosis.Frontiers in bioengineering and biotechnology · 2023Review
- Senescent cells: A therapeutic target for osteoporosis.Cell proliferation · 2022Review
- Elimination of Senescent Cells by Senolytics Facilitates Bony Endplate Microvessel Formation and Mitigates Disc Degeneration in Aged Mice.Frontiers in cell and developmental biology · 2022Article
- Enhancement of Bone-Forming Ability on Beta-Tricalcium Phosphate by Modulating Cellular Senescence Mechanisms Using Senolytics.International journal of molecular sciences · 2021Article
- Cellular senescence in musculoskeletal homeostasis, diseases, and regeneration.Bone research · 2021Review
- Antenatal Corticosteroid Therapy Attenuates Angiogenesis Through Inhibiting Osteoclastogenesis in Young Mice.Frontiers in cell and developmental biology · 2020Article
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Authors and funding
6 authors.
Funding
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Abstract
backgroundPrenatal dexamethasone exposure (PDE) induces low birth weight and retardation of fetal bone development which are associated with lower peak bone mass in adult offspring. Here we evaluated whether and how PDE affects postnatal long bone growth in mouse offspring.
methodsPregnant mice were injected subcutaneously with dexamethasone (1.2 mg/kg/day) every morning from gestational days (GD) 12-14. Femurs and tibias of 2-, 4-, 6-, and 12-week-old female offspring were harvested for histological, immunofluorescence, flow cytometric analysis, or microcomputed tomography (μCT) measurement.
resultsPDE leads to impaired bone remodeling as well as decreased bone mass in the long bone of female mouse offspring. During postnatal bone growth, significant decrease of CD45
conclusionCellular senescence mediates the toxic effect of PDE on postnatal long bone growth in mouse offspring, and inhibition of cellular senescence may be proposed for treating the retardation of bone growth caused by PDE.
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